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dc.contributor.advisorBalachandran, Siddharth
dc.creatorShubina, Maria
dc.date.accessioned2020-11-05T15:01:57Z
dc.date.available2020-11-05T15:01:57Z
dc.date.issued2020
dc.identifier.urihttp://hdl.handle.net/20.500.12613/3565
dc.description.abstractInfluenza A viruses (IAV) are negative sense RNA viruses that naturally infect a wide variety of animals. Different subtypes of the virus infect waterfowl, poultry, pigs, horses, ferrets, bats, dogs, cats and humans, causing zoonotic outbreaks and pandemics. In humans, IAV strains cause seasonal epidemics that can result in up to 50000 deaths and 700000 hospitalizations each year, and ranks in the top ten causes of death in the United States. In addition, virulent strains of IAV have caused pandemic outbreaks triggering numerous fatalities. While tropism to the upper respiratory tract is important for virus transmission, infection of the lower lung is most correlated with pathogenesis. The mammalian lung has multiple structural cell types, of which two classes are considered most important for IAV pathogenesis. These are (1) alveolar unit cells and (2) cells of the conducting airways, primarily those of the bronchi and bronchioles. Alveolar unit cells, or pneumocytes, chiefly comprise type I and type II alveolar epithelial cells, and are involved in gas exchange and surfactant production. Cells of the bronchi and bronchioles (e.g., basal, secretory, ciliated, club, goblet and neuroendocrine cells) perform numerous functions related to tissue repair/renewal, and mucous production. Upon IAV infection the regulated (or programmed) death of the infected cell represents an important pathogen clearance mechanism. Programmed cell death can be largely non-inflammatory (e.g., apoptosis) or pro-inflammatory (e.g., necroptosis). In this dissertation, I outline experiments carried out to identify the role of pro-inflammatory programmed cell death in influenza A virus clearance and pathogenesis both in vitro and in vivo. My work outlines the role of necroptosis in IAV clearance, and how this controlled form of cell death, particularly in alveolar unit cells, can be exploited as a potential new therapeutic avenue for severe influenza disease.
dc.format.extent137 pages
dc.language.isoeng
dc.publisherTemple University. Libraries
dc.relation.ispartofTheses and Dissertations
dc.rightsIN COPYRIGHT- This Rights Statement can be used for an Item that is in copyright. Using this statement implies that the organization making this Item available has determined that the Item is in copyright and either is the rights-holder, has obtained permission from the rights-holder(s) to make their Work(s) available, or makes the Item available under an exception or limitation to copyright (including Fair Use) that entitles it to make the Item available.
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.subjectCellular Biology
dc.subjectApoptosis
dc.subjectCell Death
dc.subjectInfluenza
dc.subjectNecroptosis
dc.subjectRipk3
dc.subjectSmall Molecules
dc.titleInfluenza A Virus Induced Programmed Cell Death
dc.typeText
dc.type.genreThesis/Dissertation
dc.contributor.committeememberMonestier, Marc
dc.contributor.committeememberRall, Glenn F.
dc.contributor.committeememberTempera, Italo
dc.contributor.committeememberKilpatrick, Laurie
dc.contributor.committeememberCarey, Alison J.
dc.description.departmentCancer Biology & Genetics
dc.relation.doihttp://dx.doi.org/10.34944/dspace/3547
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.description.degreePh.D.
refterms.dateFOA2020-11-05T15:01:57Z
dc.embargo.lift05/31/2026


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